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- W1531169075 abstract "Abstract IL-12 activates STAT4, which is a critical regulator of inflammation and Th1 lineage development in murine systems. The requirement for STAT4 in the generation of human Th1 cells has not been examined thoroughly. Expression of the Th1 signature markers IFNγ, IL-12Rβ2, TNFα, and CXCR3 is greatly reduced in Th1 cultures of CD4 T cells isolated from Non-Hodgkin's Lymphoma patients following autologous stem cell transplant, which have acquired STAT4 deficiency, compared to control Th1 cultures. T-bet expression is not affected whereas IL-4 and IL-5 production is increased in patient Th1 cultures. STAT4 deficiency does not result in defects in the development of Th2 cells. Reconstitution of STAT4 in patient T cells allowed recovery of Th1 signature markers IFNγ, IL-12Rβ2, and CXCR3. In contrast, ectopic expression of IL-12Rβ2 in patient Th1 cells, which was also decreased with acquired STAT4-deficiency, did not rescue STAT4 expression, though it did increase IFNγ production to levels intermediate between control and patient samples. These results demonstrate that as in murine systems, STAT4 is required for optimal human Th1 lineage development." @default.
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- W1531169075 date "2009-04-01" @default.
- W1531169075 modified "2023-10-18" @default.
- W1531169075 title "Impaired development of human Th1 cells in patients with deficient expression of STAT4 (46.14)" @default.
- W1531169075 doi "https://doi.org/10.4049/jimmunol.182.supp.46.14" @default.
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